M
Martina K. Brückner
Researcher at Leipzig University
Publications - 56
Citations - 3924
Martina K. Brückner is an academic researcher from Leipzig University. The author has contributed to research in topics: Neurodegeneration & Amyloid precursor protein. The author has an hindex of 32, co-authored 56 publications receiving 3652 citations.
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A humanized version of Foxp2 affects cortico-basal ganglia circuits in mice
Wolfgang Enard,Sabine Gehre,Kurt Hammerschmidt,Sabine M. Hölter,Torsten Blass,Mehmet Somel,Martina K. Brückner,Christiane Schreiweis,Christine Winter,Reinhard Sohr,Lore Becker,Victor Wiebe,Birgit Nickel,Thomas Giger,Uwe Müller,Matthias Groszer,Thure Adler,Antonio Aguilar,Ines Bolle,Julia Calzada-Wack,Claudia Dalke,Nicole Ehrhardt,Jack Favor,Helmut Fuchs,Valerie Gailus-Durner,Wolfgang Hans,Gabriele Hölzlwimmer,Anahita Javaheri,Svetoslav Kalaydjiev,Magdalena Kallnik,Eva Kling,Sandra Kunder,Ilona Moßbrugger,Beatrix Naton,Ildiko Racz,Birgit Rathkolb,Jan Rozman,Anja Schrewe,Dirk H. Busch,Jochen Graw,Boris Ivandic,Martin Klingenspor,Thomas Klopstock,Markus Ollert,Leticia Quintanilla-Martinez,Holger Schulz,Eckhard Wolf,Wolfgang Wurst,Andreas Zimmer,Simon E. Fisher,Rudolf Morgenstern,Thomas Arendt,Martin Hrabé de Angelis,Julia Fischer,Johannes Schwarz,Johannes Schwarz,Svante Pääbo +56 more
TL;DR: In the striatum, a part of the basal ganglia affected in humans with a speech deficit due to a nonfunctional FOXP2 allele, it is found that medium spiny neurons have increased dendrite lengths and increased synaptic plasticity, suggesting that alterations in cortico-basal ganglia circuits might have been important for the evolution of speech and language in humans.
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Plastic Neuronal Remodeling Is Impaired in Patients with Alzheimer’s Disease Carrying Apolipoprotein ε4 Allele
Thomas Arendt,Cornelia Schindler,Martina K. Brückner,Klaus Eschrich,Volker Bigl,D. Zedlick,Lena Marcova +6 more
TL;DR: Results provide direct evidence that neuronal reorganization is affected severely in patients with Alzheimer’s disease carrying the apoE ε4 allele, which might lead to a more rapid functional decompensation, thereby contributing to an earlier onset and more rapid progression of the disease.
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Changes in acetylcholinesterase and butyrylcholinesterase in Alzheimer's disease resemble embryonic development--a study of molecular forms.
TL;DR: The degeneration of the cholinergic cortical afferentation in AD as reflected by a decrease of AChE G4 is accompanied by the process of a neuritic sprouting response involved in plaque formation which is probably associated with the expression of a developmental form of the enzyme.
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Perineuronal nets potentially protect against oxidative stress
TL;DR: It is shown that neurons ensheathed by a perineuronal net in the human cerebral cortex are less frequently affected by lipofuscin accumulation than neurons without a net both in normal-aged brain and Alzheimer's disease (AD).
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Activities of key glycolytic enzymes in the brains of patients with Alzheimer's disease.
TL;DR: It is suggested that the increased activity of some glycolytic enzymes may be, at least in part, the result of the reactive astrocytosis developing in the course of AD.